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  • Title: [Recent findings regarding physiological characteristics and effects of renal dopamine].
    Author: Cuk M, Cuk D, Dvornik S, Mamula O, Manestar MM.
    Journal: Lijec Vjesn; 2004; 126(5-6):147-55. PubMed ID: 15628684.
    Abstract:
    During the past decade, it has become evident that dopamine acts not only as a classical neurotransmitter in the central and peripheral nervous system but also as an autocrine, paracrine and/or endocrine substance in peripheral, non-neuronal tissues. This work is aimed to review some of the recent aspects related to the physiological features and effects of renal origin dopamine. Renal dopamine is synthesized in the proximal tubule epithelial cells. Newly formed dopamine leaves the cellular compartment by crossing the apical cell border and the basolateral membrane side. Dopamine exerts its intrarenal action via specific cell surface receptors, differentially expressed along the nephron and other structural components of renal tissue. These receptors have been classified into five types. D1 and D5 receptors are linked to stimulation, while D2, D3 and D4 receptors are linked to inhibition of adenylyl cyclase. Renal dopamine affects electrolyte and fluid balance by regulation of renal excretion of electrolytes and water through actions on renal hemodynamics and tubular, epithelial transport. The importance of intrarenally produced dopamine as a natriuretic hormone is reflected by its capacity to inhibit the majority of sodium transporters (Na+K+ATPase, Na+/H+-exchanger) in the entire nephron. Numerous clinical and animal, experimental observations suggest that dopamine coordinates the effects of antinatriuretic and natriuretic factors and indicate that the intact renal dopamine system is of major importance for maintenence of sodium homeostasis and systemic blood pressure. Sodium retention leads to an increase in renal dopamine tonus. This function is, due to deficient renal dopamine production and/or a D1 receptor G-protein coupling defect, lost in human essential hypertension and in some animal models of genetic hypertension. A better knowledge of molecular bases of these changes may contribute to the development of specific diagnostic and therapeutic approaches in essential as well as secondary forms of hypertension.
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